Ilexsaponin A attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway

Abstract

The protective effects of ilexsaponin A on ischemia-reperfusion-induced myocardial injury were investigated. Myocardial ischemia/reperfusion model was established in male Sprague–Dawley rats. Myocardial injury was evaluated by TTC staining and myocardial marker enzyme leakage. The in vitro protective potential of Ilexsaponin A was assessed on hypoxia/reoxygenation cellular model in neonatal rat cardiomyocytes. Cellular viability and apoptosis were evaluated by MTT and TUNEL assay. Caspase-3, cleaved caspase-3, bax, bcl-2, p-Akt and Akt protein expression levels were detected by western-blot. Ilexsaponin A treatment was able to attenuate the myocardial injury in ischemia/reperfusion model by reducing myocardial infarct size and lower the serum levels of LDH, AST and CK-MB. The in vitro study also showed that ilexsaponin A treatment could increase cellular viability and inhibit apoptosis in hypoxia/reoxygenation cardiomyocytes. Proapoptotic proteins including caspase-3, cleaved caspase-3 and bax were significantly reduced and anti-apoptotic protein bcl-2 was significantly increased by ilexsaponin A treatment in hypoxia/reoxygenation cardiomyocytes. Moreover, Ilexsaponin A treatment was able to increase the expression levels of p-Akt in hypoxia/reoxygenation cellular model and myocardial ischemia/reperfusion animal model. Coupled results from both in vivo and in vitro experiments indicate that Ilexsaponin A attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway.

Cardioprotective and Anti-Aggregatory Effects of Levosimendan on Isoproterenol-Induced Myocardial Injury in High-Fat-Fed Rats Involves Modulation of PI3K/Akt/mTOR Signaling Pathway and Inhibition of Apoptosis

“…Therefore, oxidative stress burden has been implicated in the development of isoproterenol-induced changes in mitochondria, alterating the enzyme activity and transport systems and causing disturbances in cellular homeostasis. 60 -62 The present results agree with some published data that highlight the critical link between HFD/isoproterenol-induced cardiotoxicity and the development of oxidative stress burden as evidenced by the ROS generation and depression in the endogenous antioxidant system. 3,4,59 Additionally, and in harmony with other studies 17,22,23,43,63 the ischemic ameliorating effect of levosimendan and to a lesser extent cilostazol on increments in the inflammatory markers was evident.…”

Protective effects of carnosic acid against mitochondria‑mediated injury in H9c2 cardiomyocytes induced by hypoxia/reoxygenation

“…Previous findings have suggested that gypenoside protects the cardiomyocytes against the injury via the mitogen-activated protein kinase-mediated nuclear factor-κB pathway (26). In addition, as the convergent pathway of final ischemia and reperfusion injury, mitochondria-mediated apoptosis has been demonstrated to be involved in protective effects of most phytochemicals, including clematichinenoside (27) and ilexsaponin A (28).…”

The Antioxidant Activity of Pistachios Reduces Cardiac Tissue Injury of Acute Ischemia/Reperfusion (I/R) in Diabetic Streptozotocin (STZ)-Induced Hyperglycaemic Rats

“…The unstained myocardium was incubated for 30 min at 37°C in TTC (1% in 0.1 mol/L phosphate buffer, pH 7.4). The non-infarcted myocardium was deep red, in contrast to the pale of the infarcted myocardium (Zhang et al, 2017 ).…”